Nakajima Y, Nose H, Takamata A
Departments of Anesthesiology and Physiology, Kyoto Prefectural University of Medicine, Kyoto 602-0841, Japan.
Am J Physiol. 1998 Nov;275(5):R1703-11. doi: 10.1152/ajpregu.1998.275.5.R1703.
To gain better insights into the effect of dehydration on thermal and cardiovascular regulation during hyperthermia, we examined these regulatory responses during body heating in rats under isosmotic hypovolemia and hyperosmotic hypovolemia. Rats were divided into four groups: normovolemic and isosmotic (C), hypovolemic and isosmotic [L, plasma volume loss (DeltaPV) = -20% of control], hypovolemic and less hyperosmotic [HL1, increase in plasma osmolality (DeltaPosm) = 23 mosmol/kgH2O, DeltaPV = -16%], and hypovolemic and more hyperosmotic (HL2, DeltaPosm = 52 mosmol/kgH2O, DeltaPV = -17%). Hyperosmolality was attained by subcutaneous injection of hypertonic saline and hypovolemia by intra-arterial injection of furosemide before heating. Then rats were placed in a thermocontrolled box (35 degreesC air temperature, approximately 20% relative humidity) for 1-2 h until rectal temperatures (Tre) reached 40.0 degreesC. Mean arterial pressure in L decreased with rise in Tre (P < 0.001), whereas mean arterial pressure remained constant in the other groups. Maximal tail skin blood flow in L, HL1, and HL2 was decreased to approximately 30% of that in C (P < 0. 001). Tre threshold for tail skin vasodilation (TVD) was not changed in L, whereas the threshold shifted higher in the HL groups. Tre threshold for TVD was highly correlated with Posm (r = 0.94, P < 0. 001). Heart rate in the HL groups increased with rise in Tre (P < 0. 001), whereas it remained unchanged in C and L. Cardiovascular responses to heating were not influenced by V1 antagonist in C, L, and HL2. Thus isotonic hypovolemia attenuates maximal tail skin blood flow, whereas hypertonic hypovolemia causes an upward shift of Tre threshold for TVD and an increase in heart rate during hyperthermia. These results suggest that plasma hyperosmolality stimulates pressor responses in the hypovolemic condition that subsequently contribute to arterial pressure regulation during heat stress.
为了更深入了解脱水对热应激期间体温和心血管调节的影响,我们研究了等渗性低血容量和高渗性低血容量大鼠在体温升高期间的这些调节反应。大鼠被分为四组:正常血容量和等渗组(C)、低血容量和等渗组[L,血浆容量减少(ΔPV)=-20%对照]、低血容量和低高渗组[HL1,血浆渗透压升高(ΔPosm)=23 mosmol/kgH₂O,ΔPV=-16%],以及低血容量和高高渗组(HL2,ΔPosm=52 mosmol/kgH₂O,ΔPV=-17%)。在加热前,通过皮下注射高渗盐水实现高渗状态,通过动脉内注射速尿实现低血容量状态。然后将大鼠置于温度控制箱(空气温度35℃,相对湿度约20%)中1 - 2小时,直到直肠温度(Tre)达到40.0℃。L组平均动脉压随Tre升高而降低(P < 0.001),而其他组平均动脉压保持恒定。L组、HL1组和HL2组的最大尾部皮肤血流量降低至C组的约30%(P < 0.001)。L组尾部皮肤血管舒张(TVD)的Tre阈值未改变,而HL组阈值升高。TVD的Tre阈值与Posm高度相关(r = 0.94,P < 0.001)。HL组心率随Tre升高而增加(P < 0.001),而C组和L组心率保持不变。C组、L组和HL2组对加热的心血管反应不受V1拮抗剂影响。因此,等渗性低血容量会减弱最大尾部皮肤血流量,而高渗性低血容量会导致热应激期间TVD的Tre阈值上移和心率增加。这些结果表明,血浆高渗在低血容量状态下刺激升压反应,随后有助于热应激期间的动脉血压调节。